Książki na temat „Impulse response functions”

Impulsivity represents a complex multidimensional construct that may change across the lifespan and is associated with numerous neuropsychiatric disorders including substance use disorders, conduct disorder/antisocial personality disorder, and traumatic brain injury. Multiple psychological theories have considered impulsivity and the development of impulse control, inhibition, and self-regulatory behaviors during childhood. Some psychoanalytic theorists have viewed impulse control and self-regulatory behaviors as developing ego functions emerging in the context of id-based impulses and inhibitory pressures from the superego. Object relationists added to this framework but placed more emphasis on mother–child dyadic relationships and the process of separation and individuation within the infant. Cognitive and developmental theorists have viewed impulse control and self-regulation as a series of additive cognitive functions emerging at different temporal points during childhood and with an emphasis on attentional systems and the ability to inhibit a prepotent response. Commonalities exist across all of these developmental theories, and they all are consistent with the idea that the development of impulse control appears cumulative and emergent in early life, with the age range of 24–36 months being a formative period. Impulsivity is part of normal development in the healthy child, and emerging empirical data on normative populations (as measured by neuropsychological testing batteries, self-report measures, and behavioral observation) suggest that impulse control, self-regulation, and other impulsivity-related phenomena may follow different temporal trajectories, with impulsivity decreasing linearly over time and sensation seeking and reward responsiveness following an inverted U-shaped trajectory across the lifespan. These different trajectories coincide with developmental brain changes, including early maturation of subcortical regions in relation to the later maturation of the frontal lobes, and may underlie the frequent risk-taking behavior often observed during adolescence.

We examine the effect of pandemics on selected commodity prices—in particular, those of zinc, copper, lead, and oil. We set up a vector autoregressive model and analyse data since the mid-nineteenth century to determine how prices reacted to pandemics such as the 1918 Spanish Flu, 1957 Asian Flu, and 1968 Hong Kong Flu. We control for demand and supply fundamentals to generate forecasts from the point of outbreak, and we consider whether any pattern can be deduced in reactions to adverse global shocks. Results are varied, depending on choice of commodity and magnitude and type of response. No clear conclusions are possible from past pandemics, and we conclude that at the time of writing, forecasts are difficult to make in the ongoing current pandemic too. We conclude by estimating impulse response functions to assess likely impact and the subsequent response of commodity prices to the shock.

This chapter examines the principles and practice of nerve conduction studies, which constitute an extension of the clinical history-taking and physical examination, rather than a separate laboratory test. Therefore, in order to take best advantage of the physiological assessment, we need to formulate a reasonable differential diagnosis based on their clinical examination. Nerve conduction studies will help clinicians by confirming the clinical diagnosis, characterizing the neuropathic process by documenting demyelination or axonal degeneration, which dictates the speed and manner of nerve impulse propagation, localizing the site of lesions, differentiating a focal versus diffuse process, and quantitating the abnormalities by the size of the elicited response, which approximately corresponds to the number of functional nerve and muscle fibres. The chapter will appeal to those interested in a broad review of electrodiagnostic medicine and to those wanting a current update on the state-of-the art information of nerve conduction techniques.

The oligodendrocyte–myelin unit subserves saltatory conduction of the nerve impulse in the healthy central nervous system. At one time, many disease processes were thought exclusively to target the structure and function of myelin. Therefore, they were designated ‘demyelinating diseases’. But recent analyses, based mainly on pathological and imaging studies, (re)emphasize that axons are also directly involved in these disorders during both the acute and chronic phases. Another ambiguity is the extent to which these are inflammatory conditions. Here, distinctions should be made between inflammation, as a generic process, and autoimmunity in which rather a specific set of aetiological and mechanistic conditions pertain. And there are differences between disorders that are driven primarily by immune processes and those in which inflammation occurs in response to pre-existing tissue damage.With these provisos, the pathological processes of demyelination and associated axonal dysfunction often account for episodic neurological symptoms and signs referable to white matter tracts of the brain, optic nerves, or spinal cord when these occur in young people. This is the clinical context in which the possibility of ‘demyelinating disease’ is usually considered by physicians and, increasingly, the informed patient. Neurologists will, with appropriate cautions, also be prepared to diagnose demyelinating disease in older patients presenting with progressive symptoms implicating these same pathways even when there is no suggestive past history. Both in its typical and atypical forms multiple sclerosis remains by far the commonest demyelinating disease. But acute disseminated encephalomyelitis, the leucodystrophies, and central pontine myelinolysis also need to be considered in particular circumstances; and multiple sclerosis itself has a differential diagnosis in which the relapsing-remitting course is mimicked by conditions not associated with direct injury to the axon–glial unit. Since our understanding of the cause, pathogenesis and features of demyelinating disease remains incomplete, classification combines aspects of the aetiology, clinical features, pathology, and laboratory components. Whether the designation ‘multiple sclerosis’ encapsulates one or more conditions is now much debated. We anticipate that a major part of future studies in demyelinating disease will be further to resolve this question of disease heterogeneity leading to a new taxonomy based on mechanisms rather than clinical empiricism. But, for now, the variable ages of onset, unpredictable clinical course, protean clinical manifestations, and non-specific laboratory investigations continue to make demyelinating disease one of the more challenging diagnostic areas in clinical neurology.